Compound mutations in Bmpr1a and Tak1 synergize facial deformities via increased cell death
GENESIS, 56(3).
author keywords: apoptosis; facial prominence; MAP kinase; nasal septum; Smad signaling
MeSH headings : Animals; Apoptosis / genetics; Biomarkers; Bone Morphogenetic Protein Receptors, Type I / genetics; Bone Morphogenetic Protein Receptors, Type I / metabolism; Cell Death / genetics; Craniofacial Abnormalities / diagnosis; Craniofacial Abnormalities / genetics; Genetic Association Studies; Genotype; Gestational Age; Immunohistochemistry; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Transgenic; Mutation; Phenotype; Signal Transduction; Smad Proteins / metabolism; p38 Mitogen-Activated Protein Kinases / metabolism
TL;DR:
It is suggested that deletion of Tak1 aggravates the craniofacial deformities of the caBmpr1a mutants by increasing p53 and phospho‐p38 at different stage of embryogenesis.
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